The heart is a muscular organ that pumps blood throughout the body. In a normal, healthy heart the pumping is initiated by periodic electrical depolarizations that originate in the sinoatrial node. The electrical depolarizations spread throughout the myocardium, causing the heart to contract, and forcing blood into the aorta and pulmonary artery.
In healthy hearts, the myocardial depolarization occurs in a coordinated sequence, which facilitates adequate pumping. As noted, the initial depolarization generally originates in the sinoatrial node and spreads throughout the atria, thereby causing the atria to contract, forcing blood into the ventricles. Subsequently, the depolarization passes through the atrioventricular node and, through a group of specialized conducting myocardial fibers (Purkinje fibers), is transmitted through the interventricular septum and ventricles. The right and left ventricles are thus depolarized and contract to pump blood through the pulmonary artery and aorta to the body.
Heart disease is a major health problem. Numerous environmental, behavioral, genetic, and/or congenital conditions can lead to chronic or acute damage to the heart. Acute myocardial events, such as a myocardial infarction, may damage portions of the heart's native pacemakers (i.e. sinoatrial and atrioventricular nodes) or conduction systems, and may decrease the overall pumping effectiveness of the heart. Likewise, chronic conditions, such as high blood pressure, valvular disease, certain types of bacterial or viral infection, and diabetes, may produce slowly-progressing, but similarly damaging effects on the heart.
One way to treat damaged heart muscle cells is to provide pharmaceutical therapies in an effort to restore heart function. Many pharmacologic treatments are effective at improving patient quality of life by increasing cardiac output, preventing arrhythmias, and/or treating symptoms associated with heart failure. However, for some patients, pharmaceutical therapy may be ineffective or inadequate. For example, many patients who have suffered acute or chronic damage to the heart's pacemakers or conduction systems have lasting and/or recurring arrhythmias. Often these arrhythmias result in a loss of chronotropic competence, and consequently these patients are unable to modulate their intrinsic heart rate in response to changing metabolic demands. In addition, in some patients, conduction through the ventricles may be abnormal or intermittent and/or the depolarizations may be asynchronous, whereby contractions of the atria and ventricles are poorly coordinated. Further, many patients have difficulties complying with pharmaceutical regimens. All these conditions may have a deleterious effect on cardiac output, may contribute to the progression of cardiac disease, and may ultimately lead to death.
For many patients, implantable cardiac rhythm management systems (e.g. pacemakers, cardiac resynchronization pacemakers and/or defibrillators) are necessary. Pacemakers generally include a housing (can) that encloses various electrical components, such as a battery, control hardware, communications systems, and/or other diagnostic components. The pacemaker also includes a number of leads and electrodes, which interface with portions of the heart to be stimulated or regions of the heart where physiological signals are sensed. Numerous different pacemakers and/or defibrillators are available, and the specific type of device is selected based on a variety of clinical factors that are evaluated by a physician.
More recently, there has been growing interest in developing pacemakers using cellular sources, which may be implanted or injected into certain regions of the heart to produce a new, biological pacemaker. The cells may be engineered to have electrical properties that mimic natural cardiac pacemakers, but may be implanted at a variety of cardiac locations and may be selected based on particular patient needs. However, the use of biological pacemakers may present some limitations, and even with a biological pacemaker, many patients may still benefit from an implantable device. For example, the biological pacemaker may have inherent limits on cardiac rates that it can achieve, and an implantable device may be needed when higher metabolic demands are encountered. Further, a biological pacemaker may be temporarily or permanently affected by medications or any condition that may affect normal myocardial cells (e.g. infarction). In addition, an implantable device may be desired to monitor, record, and/or transmit information related to patient status, including biological pacemaker status, to healthcare professionals to facilitate continued treatment.
For some biological pacemaker system designs, the biological pacemaker may not begin to provide appropriate rhythm and rate control until some time after implantation. During this time, an implantable electrical pacemaker may be used. However, as the biological pacemaker begins to function and take over the intrinsic pacemaking activity of the heart, it would be useful to determine if sensed cardiac depolarizations originate in the implantable electrical pacemaker, in the biological pacemaker, in an ectopic cardiac site, or in the native pacemaker. In addition, it may be necessary to slowly phase in the biologic pacemaker therapy. This may be desirable when a newly implanted biologic pacemaker has yet to establish reliability, to prevent an abrupt change in demands on the heart due to a rapid change in pacing rate, to facilitate formation of necessary electrical connections between native cardiac tissue and an implanted biologic pacemaker, and/or to provide a back-up pacing should a new biological pacemaker fail to adequately pace the heart.